Over the last 10 years, there has been a significant increase in ankle MRI. When patients present to their primary care physician or specialist with ankle or hindfoot pain, there are a variety of possible etiologies. Unfortunately, these different diagnoses have overlapping clinical signs and symptoms. For this reason, referring clinicians tend to rely on MRI to clarify or solidify a diagnosis to guide treatment and management decisions. Therefore, it is important for the radiologist to be able to recognize and diagnose common pathologies within this region. This review article focuses on ligamentous injuries, common tendon pathology, and overuse syndromes.
Ankle joint injuries are the most common sports-related injuries with approximately 75% involving the lateral ligamentous complex.1 The lateral complex is composed of the anterior talofibular ligament (ATF), the calcaneofibular ligament (CF), and the posterior talofibular ligament (PTF).1 The anterior talofibular ligament is the most commonly injured ligament as it is the weakest of the lateral ankle ligaments, followed by the calcaneofibular ligament and finally the posterior talofibular ligament.1-3 These ligaments are almost always injured sequentially from anterior to posterior. Therefore, if the ATF is intact on imaging, it can often be presumed that the other lateral collateral ligaments are also intact.4
Nearly half of ATF injuries occur during an athletic activity with basketball being the most commonly involved sport.5 The classic mechanism of injury is ankle inversion with forced plantar flexion. Patients typically present with acute lateral ankle pain and soft tissue swelling.1,6 Clinicians evaluate the degree of swelling, ecchymosis, and inability to bear weight to assess the grade/extent of ligamentous injury.1,6 Teenagers and young adults experience the highest rates of ankle sprains with an equal incidence among males and females.1,3,7
The mainstay treatment for acute ligamentous ankle injury is conservative management with short-term immobilization, followed by functional rehabilitation. A successful recovery occurs in approximately 80% of patients utilizing this approach.1,3,7 Since treatment rarely requires surgical intervention, MRI is typically reserved for evaluating highly competitive athletes in whom primary ligamentous repair is being considered, as well as for the 20% of patients who develop chronic ankle instability following failed conservative treatment.1-3, 7
When evaluating the lateral ligaments, both the axial and coronal images are useful. Axial images demonstrate the ATF and PTF more clearly, while coronal images better demonstrate the calcaneofibular ligament. MRI findings of acute ATF injury include ligament discontinuity, nonvisualization of the ligament, detachment, and/or contour irregularity.2-4 Indirect associated findings for an ATF injury include loss of surrounding fat planes, ankle joint effusion, and lateral soft tissue edema.2-4 In addition, the presence of a “bright rim” sign (a bright dot-like or curvilinear high-signal intensity focus on T2 images involving the talus and fibula along the cortex) significantly increases the accuracy of detecting ATF injuries.3 A complete tear is typically seen on MRI as a fluid-gap/discontinuity with subsequent retraction of lax fibers or nonvisualization of the ligament (Figure 1).7
The deltoid ligamentous complex, also known as the medial collateral ligament, is the strongest of the ankle ligaments. It serves as the primary stabilizer of the axially loaded ankle.6,8 Unlike its lateral counterpart, it is rarely injured, accounting for only 5% of all ankle sprains. Male athletes are 3 times more likely to experience a medial ankle sprain than females.6-9 Forced eversion and pronation of the ankle is the classically described mechanism of injury, most often resulting in a medial malleolus avulsion fracture due to the strength of the deltoid ligament.6,8 Medial ankle sprains are more painful than lateral ankle sprains and often result in mechanical instability.7 Patients commonly present with medial ankle hematoma and tenderness in the acute setting.8
The deltoid ligament is comprised of 2 obliquely oriented, parallel components (superficial and deep), which join together to form the triangular/deltoid-shaped ligamentous complex.6-9 These 2 components act somewhat synergistically to stabilize the ankle against valgus and pronation forces.8 The most superficial component is comprised of the tibiocalcaneal, tibionavicular, posterior superficial tibiotalar, and tibiospring ligaments. The deep group consists of the anterior tibiotalar ligament and posterior deep tibiotalar ligaments (PDTL).8 Tears involving the deep ligaments are more common; however, tears of both layers rarely occur in isolation. Injuries to these two components should be classified separately on MRI.7,8,10
When evaluating the deltoid ligament, the coronal images are typically the easiest to use. The most common MRI findings of acute deltoid ligament sprain include fascicular disruption, heterogeneity, and loss of striations within the ligament.10 An acutely torn ligament is best appreciated on fluid-sensitive, fat-saturated sequences in the coronal plane, which demonstrate increased fluid signal with fluid-filled gaps or complete discontinuity of the ligament (Figure 2).7,10 The deep PDTL is generally regarded as the thickest and strongest of the ligaments and normally demonstrates a heterogeneous appearance with internal striations caused by individual fascicles separated by interposed fat; acute injury causes this ligament to become amorphous with loss of these striations secondary to hemorrhage and hemosiderin deposition.7,10 Treatment of deltoid ligament injuries remains somewhat controversial with surgical treatment being primarily reserved for those with associated fractures, chronic deltoid ligament injury, and/or chronic ankle instability.8,10
Tendons should have a homogeneous hypointense appearance on MRI. Specifically, T1-weighted (T1W), T2-weighted (T2W), proton density (PD), and inversion recovery (IR) images should all demonstrate homogeneous hypointense signal intensity throughout the tendons. The Achilles tendon is the one exception to this rule within the ankle (see Achilles discussion below). Since the Achilles tendon is a conglomeration of tendons, it often has some small foci of intermediate intratendinous signal intensity. When reviewing an MRI, the best approach is to follow each tendon from the most cranial image to the most caudal image, evaluating them for homogeneity with regard to shape and signal intensity. It is the opinion of the authors that the axial plane provides the easiest approach for evaluating tendons of the ankle.
The major abnormalities involving tendons include degeneration, tenosynovitis, partial tears, complete tears, tumors, and a multitude of deposition disorders within the tendon. Degeneration of a tendon occurs from aging or chronic overuse. Generally, this is a painless process but may evolve or predispose the tendon to partial or complete rupture with relatively minimal trauma. Tendons with degeneration will exhibit a normal or enlarged caliber with intermediate signal intensity within the substance of the tendon (centrally) on T1 sequences and corresponding hyperintense T2 signal. Tendinitis, tendinopathy or tendinosis are all used to describe abnormal intratendinous signal. On imaging, it is difficult or impossible to distinguish signal intensity of degeneration from partial tears, and both processes are thought to be on a continuum of micro-tear progression.11
Tenosynovitis refers to fluid surrounding the tendon, which indicates an inflammatory process of the tendon sheath. The underlying tendinous substance can be of normal or abnormal signal intensity. Fluid signal intensity (hypointense T1/hyperintense T2) must surround the entire circumference of the tendon to diagnose tenosynovitis.
A partial tear represents incomplete disruption of the tendon fibers, whereas a complete tendon tear/rupture results in total disruption of the tendon with 2 distinct ends of the tendon identified. Partial tears can be variable in appearance on MRI but typically exhibit high signal intensity within the tendon substance on fluid sensitive sequences. Chronic tears may have low T2 signal intensity due to scarring and fibrosis. The tendon may appear thickened, thinned, or of normal caliber depending on the etiology and age of the injury. A tear may occur in a vertical or longitudinal fashion with respect to the long axis of the tendon.
A complete rupture is easier to identify on clinical examination secondary to dysfunction or severe weakness. The role of imaging is to confirm the presence of a full thickness tear, determine the quality of tendon remnants, and identify the degree of retraction. These factors are important for patient management and surgical planning.11
Achilles tendon pathology is a common cause of hindfoot pain. In the past 3 decades, the incidence has increased secondary to increased participation in recreational and competitive sports.12 The rate of Achilles tendon injuries in runners is approximately 10 times higher than in age-matched controls.13 The most common patients who suffer from this condition are physically active individuals who have recently increased their training regimen, resulting in repetitive microtrauma. The peak age of occurrence is 30-40 and with a slight male predominance.14 As the largest tendon in the body, the Achilles tendon endures strain and is at risk of rupture from running, jumping, and sudden acceleration and deceleration movements.14 Achilles tendon injury can be associated with trauma at any age, and physical examination findings typically differentiate between partial and complete rupture.14
Achilles tendon rupture presents with an acute onset of severe pain, often described as “being kicked” or “shot in the heel.”12 In contrast, pain associated with tendinopathy generally occurs at the beginning and end of a training session with variable periods of discomfort during activity.13 Tendon injuries can be acute or chronic. In the acute phase, the tendon becomes edematous with maximal tenderness to palpation approximately 2-6 cm proximal to the insertion point on the calcaneus.13 Patients will have difficulty with active plantar flexion of the foot. The “Thompson test” or squeezing of the calf muscle with the patient in a prone position assesses the integrity of the Achilles tendon. If intact, calf squeeze will result in passive plantar flexion. In the setting of Achilles rupture, however, the test will not result in passive plantar flexion.14
The Achilles tendon represents a confluence of the gastrocnemius and soleus muscles that end in a tendinous insertion on the superior calcaneal tuberosity.13 The tendon most commonly has a flat or concave anterior margin on axial images; however, a focal convexity may be seen as a normal variant in some individuals. This focal anterior contour convexity is caused by the soleus muscle fibers merging with the gastrocnemius muscle in a spiral configuration.11 The tendon does not have a surrounding true synovial sheath, as is the case with the remaining tendons of the ankle; rather, it has a paratenon composed of a single layer of cells. This surrounding tissue is highly vascularized and is responsible for much of the blood supply to the tendon. Approximately 12-15 cm from its insertion point onto the calcaneus, the fibers begin to rotate at 90 degrees, and this rotation becomes most pronounced at approximately 5-6 cm from the insertion. Angiographic injection studies have demonstrated a zone of relative hypovascularity 2-7 cm proximal to the insertion point. This predisposes the distal aspect of the tendon (approximately 4-6 cm proximal to the calcaneal insertion) to injury with a relative inability to properly heal.11,13
The Achilles tendon is easiest to evaluate utilizing both the sagittal and axial planes. The sagittal plane demonstrates continuity of a normal tendon with a uniform slender appearance (Figure 3A). Acute partial thickness injury will manifest as edema and hemorrhage, which is seen as increased intra-tendinous T2 signal intensity. In addition, the aforementioned flat to concave anterior margin will appear convex anteriorly, which is best seen on the axial images. A focal anterior bulge may be seen with both tendinosis and partial tears on sagittal sequences (Figure 3B). In the setting of complete tendon rupture, the most reliable imaging finding is identifying tendon discontinuity (Figure 3C). When viewed in the sagittal plane the degree of retraction may also be evaluated which is important for surgical planning. A complete tear or rupture generally requires surgical intervention, while a partial tear may be amenable to conservative therapy.11
The medial compartment tendons of the ankle from anterior to posterior include the posterior tibialis, flexor digitorum, and flexor hallucis longus (remembered as Tom, Dick and Harry). Flexor hallucis longus (FHL) tenosynovitis is commonly referred to as “dancer’s tendinitis” due to its high prevalence among professional female ballet dancers.15,16 Chronic, repetitive, forced plantar-flexion, such as en-pointe dancing, creates irritation and inflammation of the flexor hallucis longus tendon sheath as it enters the flexor retinaculum. This leads to the development of tenosynovitis, the most common FHL-related injury.15,16 Patients classically present with insidious onset posteromedial ankle pain that is worsened by activity.16 The hallmark physical exam finding is pain with active hallux plantar flexion against resistance.16,17
Tenosynovitis most commonly occurs proximally, posterior to the talus, at the level of the sustenaculum talus as the tendon descends into the fibro-osseous tunnel between the medial and lateral talar tubercles.2,17,18 Symptoms, however, may occur anywhere through-out its course, including the midfoot at the master knot of Henry and distally within the forefoot between the sesamoids at the region of the FHL tendon insertion.2,17,18 Therefore, it is essential for the radiologist to follow the FHL tendon from its origin to its insertion in order to avoid overlooking less common but symptomatic locations of irritation. One of these uncommon areas is at the knot of Henry (Figure 4). The master knot of Henry is the midfoot tendinous junction or crossing between the flexor hallucis longus and flexor digitorum longus,19 originally described by Henry. There is typically FHL tenosynovitis proximal to the master knot. Various additional pathologies have been described in association with FHL tenosynovitis, such as posterior ankle impingement, which may be caused by a mobile os trigonum or Stieda’s process (see section on os trigonum syndrome), synovial adhesions, tendon hypertrophy, distal insertion of the FHL muscle, muscle elongation, longitudinal degenerative tears, and nodularity within the fibro-osseous tunnel.16,17
MRI is often ordered if there is a high clinical suspicion for posterior impingement or FHL tenosynovitis.16 One study demonstrated 82% of patients with suspected FHL tenosynovitis had positive MRI findings, revealing excess fluid accumulation within the FHL tendon sheath posterior to the ankle joint (Figure 5).16 A potential pitfall is a normal communication between the FHL tendon sheath and tibiotalar joint that exists in approximately 20% of individuals. Care should be taken not to mistake physiologic synovial fluid occurring within the tendon sheath in these individuals with pathology (Figure 6).2, 20
Conservative treatment with physical therapy and anti-inflammatory medication is often the appropriate initial treatment for FHL tenosynovitis. Surgical intervention is typically reserved for high-level athletes and performers unable to perform desired activities or in the setting of failed conservative management.16 The surgical technique utilized for FHL tenosynovitis is tendon sheath release.16
The posterior tibial tendon (PTT) is the largest tendon within the medial compartment and is approximately twice the size of the others (flexor digitorum and flexor hallucis longus). The PTT passes inferior and posterior to the medial malleolus and uses the medial malleolus as a pulley. The PTT attaches to the navicular bone, the 3 cuneiforms, and the bases of the first through fourth metatarsals. A potential pitfall in evaluating this tendon is the multiple sites of attachment and orientations of the multiple tendinous branches. The attachment sites often have a thickened appearance and high signal intensity, which is a normal finding and should not be confused with a partial tear, especially at the navicular attachment site. 11
High signal intensity or tendinous thickening elsewhere in the tendon, however, is considered pathologic. Hyperintense intrasubstance T2 signal intensity indicates a partial tear (Figure 7). Commonly, this will be evident as the tendon passes posterior to the medial malleolus, as this is a site of bony compression with a forced eversion type injury.21 A small amount of fluid may be present eccentrically around a normal tendon. If fluid is seen completely encompassing the tendon, this implies a tenosynovitis. A high association of PTT dysfunction is associated with abnormalities of the navicular bone, to include os naviculare, and will be discussed in more detail elsewhere in this article.
Classically, 3 tendons are found in the anterior compartment of the ankle. From medial to lateral, these are the anterior tibial, extensor hallucis longus, and extensor digitorum longus (can be remembered as “Tom’s Hairy Dog”). These tendons are responsible for dorsiflexion of the ankle and foot. The anterior tibial tendon is the most likely of all of the anterior compartment to be pathologic. This tendon is the most medial and the largest of the anterior tendons. It begins at approximately the junction between the lower and middle third of the tibia and courses inferiorly to the medial border of the foot, inserting on the first metatarsal base and first cuneiform. Throughout its course, it is held tightly to the ankle joint by three retention tunnels formed by the superior extensor retinaculum and the superiormedial and inferiomedial limbs of the inferior extensor retinaculum.23
Trauma is a common cause of anterior tibial tendon injury. Non-traumatic tears are uncommon, but may be seen with increasing age and in individuals who run on inclines. Rupture can result in a significant degree of dysfunction with diminished ankle dorsiflexion strength. Occasionally, patients with a partial or complete tear of this tendon present with a focal mass suspected to be a tumor, rather than with symptoms of a tendon injury, but most are diagnosed clinically prior to imaging. 11 On physical exam, weak dorsiflexion of the ankle with maintained hyperextension of the hallux and lesser digits will be evident.24
The role of imaging with a complete anterior tibial tendon rupture is for confirmation, to detect other tendinous injuries, to evaluate the extensor retinaculum, and for surgical planning. The classic MR findings of any tendon rupture is discontinuity of the tendon, thickening of the retracted portion, and excess fluid in the tendon sheath (Figure 8).24
Nonsurgical treatment includes bracing and is reserved for the elderly or cases in which surgery will not be tolerated secondary to medical comorbidities.25
The lateral compartment tendons of the ankle include the peroneus brevis and longus (also known as the fibularis brevis and longus), which serve as the primary evertors of the foot. Together, they pass posterior and inferior to the lateral malleolus and use this bony prominence as a pulley. A common tendinous sheath is shared in the proximal fibula; the tendons and sheath then separate distally to become 2 distinct tendons. The peroneus brevis attaches to the base of the fifth metatarsal. The peroneus longus splays out to attach on multiple sites along the plantar aspect of the foot, mainly involving first cuneiform and first metatarsal. Normally, the peroneus brevis is flat or oval shaped. It is situated posterior to the lateral malleolus and anterior to the peroneus longus.
“Peroneus brevis split” is used to describe a longitudinal or vertically oriented tear, which is the most common injury of the peroneus brevis tendon. A history of severe or recurrent inversion type ankle injury is usually elucidated. Lateral ankle pain and edema along the course of the tendon is generally evident clinically. Multiple structures, to include the lateral collateral ligaments, have a high association of injury with peroneus brevis injuries, and many symptoms overlap with chronic ankle instability.11 During forced dorsiflexion, the peroneus brevis tendon is compressed between the peroneus longus and the lateral malleolus, resulting in a vertical tear. The key findings of a split tear on MRI include identifying the peroneus brevis tendon separated into 2 distinct tendons (Figure 9).
Also known as posterior impingement syndrome, os trigonum syndrome (OTS) presents as acute or chronic posterior ankle pain exacerbated by both plantar and dorsiflexion. Along with other ankle impingement syndromes, OTS is most commonly seen in dancers and soccer players.26,27 The name os trigonum syndrome infers causation of a prominent os trigonum (an unfused accessory ossicle of the lateral tubercle of the talus), but this is only one of the anatomic etiologies. Other predisposing anatomic variants include a prominent lateral talar tubercle termed “Stieda’s process” (a shelf-like superior prominence of the calcaneal tuberosity), prominent down-sloping of the posterior tibial articular surface, and a posterior intermalleolar ligament.28,29 Soft-tissue causes of impingement can also occur and may be attributed to synovitis of the flexor hallucis longus tendon sheath, a thickened posterior intermalleolar ligament, posterior synovial recess of the subtalar and tibiotalar joints, disruption of the synchondrosis between the os trigonum and the lateral talar tubercle, or loose bodies.28-34
An os trigonum may be present in up to 14% of asymptomatic patients.32 Therefore, MRI is critical in assessing for findings of OTS, including bone marrow edema, posterior ankle soft tissue inflammatory changes, a thickened posterior intermalleolar ligament, and posterior ankle synovitis (Figure 10). Inflammatory changes are specifically seen in the posterior synovial recess of the subtalar and tibiotalar joints.29 Synovitis of the flexor hallucis longus is also commonly seen. Additional imaging findings on MRI include posterior capsular thickening, bone marrow edema or fluid signal at the synchondrosis, and ligament disruption. After diagnosis of OTS, conservative management, which may include image-guided steroid injection, is the first line of treatment. If conservative management fails, arthroscopic resection of the os trigonum or other associated abnormalities is performed.
Os naviculare syndrome is generally classified as a chronic stress related injury. Although there is no classic patient population, the symptoms of os naviculare syndrome become more pronounced during weight-bearing, walking, repetitive activities, and when wearing narrow shoes.35 There are three types of accessory navicular bones that are classified based on their shape and location. Type I is located in the distal portion of the posterior tibial tendon, measuring 2-3 mm and is usually asymptomatic. Type II is most important clinically as it is present in up to 4%-21% of the population and is commonly associated with medial bone pain.36 Considered the secondary ossification center of the navicular bone, a type II accessory navicular bone resides slightly posterior to the medial pole of the navicular bone (Figure 11). This accessory bone has also been referred to as a “prehallux.” Type III is sometimes referred to as a fused Type II and relates to a prominent navicular tuberosity. Further discussion relates to Type II accessory navicular bones, as it is the most common type to cause pain.
Repetitive actions may cause shearing stress forces at the ossicle-navicular synchondrosis. Since all or portions of the posterior tibial tendon insert on the accessory ossicle, this may lead to tenosynovitis of the posterior tibial tendon, tendon disruption, granulomatous inflammation, soft tissue swelling, and/or a mass of fibrocartilage tissue. Sequelae of chronic shearing forces at the synchondrosis include inflammation and osteonecrosis.
The MRI findings include bone marrow edema of both the medial pole and posterior aspect of the navicular bone, as well as within the accessory ossicle (Figure 12). Destruction of the cartilaginous cap may sometimes be seen as high signal intensity on fat suppressed fluid sensitive sequences. Indirect findings include widening of the ossicle-navicular synchondrosis or fracture of the accessory ossicle. Definitive treatment is surgical intervention, as untreated patients may go on to develop flatfoot, instability, and/or altered gait mechanics.36,37
Haglund syndrome (HS) was first described in 1927 by Patrick Haglund.38 HS is a chronic overuse syndrome characterized by a chronic inflammatory process with soft tissue irritation or compression by a “Haglund deformity.” The Haglund deformity (also known as pump bump or Bauer bump) refers to hypertrophy of the posterior superior calcaneus, which compresses the Achilles tendon between it and footwear. Patients usually present with posterior heel pain that occurs when starting to walk after a period of rest.38 Haglund syndrome is characterized clinically by painful soft tissue swelling, the so-called “pump bump,” at the level of the Achilles tendon insertion.39 Haglund syndrome is more commonly seen in women secondary to wearing tight fitting footwear, “pumps.”38 Hindfoot varus, low back shoes, and pes cavus are all predisposing factors.38 The condition results in mechanically induced inflammation of the superficial bursa, Achilles tendinosis (bump), retrocalcaneal bursitis (bump) due to repetitive compression from the back of the shoes (pumps), and prominent bursal projection of the calcaneus (bump) .38
On MRI, the diagnosis is most readily made utilizing the sagittal plane. Both T1 and fluid sensitive sequences are useful. The classic triad of findings include retrocalcaneal bursitis, Achilles tendinosis or partial tear, and retro Achilles bursitis (Figure 13). Occasionally, bone marrow edema may be seen within the posterior calcaneus involving Haglund’s deformity. Treatment for this syndrome is conservative with a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids. Patients may also respond to a minimally invasive procedure with ultrasound-guided local injection into the retrocalcaneal bursa. Surgical treatment can also be performed with bursectomy and resection of the Haglund deformity.38
Anterior impingement syndrome (AIS) is a common cause of chronic ankle pain caused by altered joint biomechanics. The classic demographic includes avid soccer players and ballet dancers.28 These patients usually present with limited and painful dorsiflexion secondary to mechanical impingement by osteophyte formation of the anterior tibial plafond and anterosuperior talus that collide in dorsiflexion, resulting in soft-tissue impingement (Figure 14A). Soft-tissue impingement by hypertrophied synovium has also been implicated. As to the cause of the osteophyte formation, many mechanisms have been proposed. The current general consensus is that it is multifactorial.28 A possible mechanism of injury is repetitive forced dorsiflexion leading to repeated microtrauma, trabecular microfactures, and periosteal hemorrhage with subsequent new bone formation at the site of injury.28,29 Another postulated mechanism is traction of the anterior capsule during plantar flexion causing avulsion injuries.28,29
MRI is particularly useful in detecting bone marrow edema, synovitis, and soft-tissue thickening within the anterior recess (Figure 14). MRI can also aid in assessing the degree of cartilage damage.28,29,40 Other findings on both conventional weight-bearing radiographs and MRI include narrowing of the tibiotalar joint space, anteriomedial tibial and talar osteophytes, and soft tissue swelling of the anterior compartment. Lastly, an anterior tibotalar degree of < 60o may indicate anterior impingement syndrome.28 Treatment usually begins with conservative management, including physical therapy, limitation of range of motion, and correction of over pronation. If conservative management fails, arthroscopy or open surgery may be performed to remove the osteophytes and soft tissue abnormalities.
There are a myriad of causes of ankle and hindfoot pain with ligamentous injury, tendon injury, and overuse syndromes being among the more common etiologies. It is imperative for the radiologist to have a working knowledge of normal anatomy, anatomic variants that mimic pathology or predispose patients to injury, and the spectrum of imaging findings of multiple pathological conditions on various modalities. Applying this knowledge when interpreting imaging studies — particularly MRI — will aid the referring clinician in making the most appropriate treatment decisions.
MRI of Ankle and Hindfoot Pain. J Am Osteopath Coll Radiol.
